Exam 21 - Basic EKG

• Cardiac electrophysiology focuses on the heart's electrical properties and how they relate to its function, including how dysrhythmias are interpreted and managed

Basic Concepts of Cardiac Electrophysiology

• Automaticity refers to the heart muscle's ability to contract rhythmically on its own
• Irritability is heart muscle's ability to respond to stimuli, similar to nerve cells
• Conduction system control means the autonomic nervous system regulates heart's conduction system

Sympathetic Nervous System

• Increases heart rate through epinephrine and morepinephrine release

Parasympathetic Nervous System

• Decreases heart rate through acetylcholine release
• Hormone/ion concentrations and body temperature affect heart function, plus impulse conduction, heartbeat initiation, and coordination between atria and ventricles

Impulse Generation and Conduction Pathway

• SA Node is heart's natural pacemaker, generating impulses at 60-100 bpm, located in upper right atrium
• Atrial Pathways conduct impulses through both atria via Bachmann's bundle and internodal pathways, causing atrial contraction
• AV Node slows impulses to allow atrial contraction and ventricular filling, capable of generating impulses at 40-60 bpm if the SA node fails, resides at base of right atrium
• Bundle of His conducts impulses from AV node, splitting into right and left bundle branches
• Purkinje Fibers are a network of fibers causing ventricular contraction, can generate impulses at 20-40 bpm if higher nodes fail

Basics of Dysrhythmia Analysis

• Dysrhythmia refers to any cardiac rhythm disturbance deviating from normal sinus rhythm
• Accurate analysis and treatment of dysrhythmia improves patient safety and outcomes
• Nursing role in dysrhythmia analysis includes cardiac monitoring, lead selection, and rhythm interpretation

Electrocardiogram (ECG/EKG)

• Records the heart's electrical activity, showing transmission of cardiac impulses through the myocardium
• Normal conduction occurs downward, from the right side of the heart to the left leg, Lead II
• Depolarization refers to electrical impulse movement causing muscle contraction
• Repolarization is recovery phase during diastole (heart muscle at rest); atrial repolarization isn't visible on ECG because it occurs during ventricular depolarization

ECG Paper

• The horizontal axis on ECG paper measures time, where 1 mm square equals 0.04 seconds and 5 mm square equals 0.20 seconds
• The vertical axis on ECG paper represents voltage, where 1 mm grid interval represents 1 millivolt

ECG Leads

• Limb leads are I, II, and III, placed on arms and legs
• 5-lead systems monitor all limb leads and one chest lead
• 12-lead ECG provides 12 different views of the heart
• Precordial leads have six leads (V1-V6) positioned on chest wall for a horizontal plane view of cardiac activity

Precordial Lead Placement

• V1: fourth intercostal space, right sternal border
• V2: fourth intercostal space, left sternal border
• V3: midway between V2 and V4
• V4: fifth intercostal space, mid-clavicular line
• V5: fifth intercostal space, anterior axillary line
• V6: fifth intercostal space, mid-axillary line

PQRST Complex

• PQRST complex represents cardiac electrical activity on graph paper
• P wave stands for atrial depolarization
• Q wave is the first negative deflection after P wave, pathological if >0.04 seconds or more than ¼ height of R wave
• R wave represents the first positive deflection after the P wave
• S wave has a negative deflection after the R wave
• QRS complex stands for ventricular depolarization (contraction), plus normal duration is 0.06-0.10 seconds
• PR interval represents time for impulse travel from the SA node to the AV node fibers, normal duration is 0.12-0.20 seconds
• T wave stands for ventricular repolarization
• ST segment marks early repolarization of the ventricular muscle

ECG Interpretation Steps

• To determine heart rate, assess whether it's fast, slow, or normal
• Six-second method of heart rate determination counts R waves in a 6-second tracing and multiplies by 10
• 300 method (large box method) determines heart rate by dividing 300 by the number of large boxes between two R waves
• 1500 method (small box method) determines heart rate by dividing 1500 by number of small boxes between two R waves
• To determine rhythm (regularity), assess R-R and P-P intervals
• Next, find and assess P waves including configuration, presence, and relation to the QRS complex, and measure the P-R interval, which should be 0.12-0.20 seconds

Measuring ECG Components

• The QRS complex should measure 0.06 - 0.10 seconds
• You should find and assess T waves, noting any positive or negative deflections
• Evaluate the ST segment (only relevant with a 12-lead ECG), where depression indicates myocardial ischemia / elevation indicates damage/infarction
• QT interval should measure ½ of the R-R interval

Common Dysrhythmias

• Dysrhythmias are caused by altered impulse formation/transmission or myocardial cell irritability
• Normal Sinus Rhythm (NSR) has a rate of 60-100 bpm, a regular rhythm, a P wave present for each QRS complex with normal/identical configuration, a normal P-R interval (0.12-0.20 seconds) and a normal QRS interval (0.06-0.10 seconds), and an upright T wave

Sinus Rhythms

• Sinus Tachycardia has a rate >100 bpm (up to 150 bpm or more) with a regular rhythm. P waves are present for each QRS complex with normal configuration, and each P wave is identical. The P-R interval is normal, the QRS complex is normal, and the T wave is normal.
• Sinus Tachycardia's etiology is sympathetic nervous system stimulation
• Causes of Sinus Tachycardia include exercise, anxiety, fever, shock, medications, heart failure, caffeine, drugs, and tobacco
• Clinical manifestations of Sinus Tachycardia include palpitations, decreased cardiac output, hypotension, and angina
• Medical management of Sinus Tachycardia is treating the root cause
• Sinus Bradycardia has a rate of <60 bpm with a regular rhythm. P waves are present for each QRS complex, with normal configuration, and each P wave is identical. The P-R interval is normal, the QRS complex is normal, and the T wave is normal.
• Sinus Bradycardia's etiology is parasympathetic nervous system stimulation
• Causes of Sinus Bradycardia include sleep apnea, intracranial tumors, myocardial infarction, medications, carotid sinus massage, vasovagal stimulation, endocrine disorders, hypothermia, and potentially normal for athletes
• Clinical manifestations of Sinus Bradycardia include fatigue, hypotension, lightheadedness, and syncope
• Medical management of Sinus Bradycardia involves treating the cause and maintaining cardiac output; atropine and transcutaneous pacing may be necessary

Supraventricular Tachycardia

• Supraventricular Tachycardia (SVT) has a rate of 150-250 bpm with a regular rhythm; plus, P waves may or may not be present for each QRS complex and normal P-R interval, QRS complex, and a normal T wave
• Etiology of Supraventricular Tachycardia is rapid rhythm from ectopic foci in the atria
• Causes of Supraventricular Tachycardia include medications, alcohol, mitral valve prolapse, sympathetic response, and hormonal imbalance
• Clinical manifestations of Supraventricular Tachycardia include palpitations, angina, lightheadedness, and dyspnea
• Medical management for Supraventricular Tachycardia includes assessing patient stability; treatments include carotid sinus pressure, medications (adenosine, digoxin, beta blockers, calcium channel blockers, or amiodarone), or catheter ablation

Atrial Rhythms

• Atrial Flutter has an atrial rate of 250-300 bpm with a regular or irregular rhythm. P waves have a saw-toothed pattern. The PR interval is not measurable, QRS complex is normal and T wave is not measurable
• Etiology of atrial flutter involves single irritable focus in the atria Causes of atrial flutter include lung disease, ischemic heart disease, hyperthyroidism, hypoxemia, heart failure, and alcoholism
• Atrial Fibrillation has an atrial rate that is unmeasurable (350-600 bpm) plus an irregularly irregular rhythm. P waves are not recognizable and P-R interval is unmeasurable. The QRS complex and T waves are normal.
• Etiology involves multiple ectopic foci in the atria
• Causes include cardiac surgery, acute MI, hypertension, pulmonary embolism, atherosclerosis, mitral valve disease, heart failure, cardiomyopathy, congenital abnormalities, COPD and thyrotoxicosis
• Clinical manifestations common to both atrial flutter and fibrillation include palpitations, dyspnea, angina, lightheadedness, syncope, and fatigue
• Medical management common to both includes treating atrial irritability; slowing ventricular response, correcting the primary cause. Anticoagulation therapy (heparin, warfarin) and pharmacologic treatments (calcium channel blockers, beta blockers, digoxin, and amiodarone) are crucial. Cardioversion may be considered; catheter ablation can be performed.

Atrioventricular Blocks

• Atrioventricular (AV) block indicate defects in the AV node slowing/impairing conduction
• First-degree AV block has a prolonged PR interval (> 0.20 seconds) with all other measurements normal
• Aging, ischemic, and valvular heart disease can cause first-degree AV block
• There are generally no significant clinical manifestations associated with first-degree AV block
• First-degree AV block requires no treatment
• Second-degree AV block, Type I (Mobitz I / Wenckebach) has a regular P-P interval, erratic R-R interval, and more P-waves than QRS complexes. PR interval is variable, QRS complex is normal for conducted beats, and T wave is normal.
• Second-degree AV block, Type I (Mobitz I/Wenckebach) etiology is progressive lengthening of the PR interval until a QRS complex is dropped
• Causes include aging, AV nodal-blocking drugs, acute inferior wall MI, ischemic heart disease, and digitalis toxicity
• Clinical manifestations are usually well tolerated unless bradycardia exists, and medical management involves discontinuing contributing drugs, but a pacemaker may be considered
• Second-degree AV block Type II (Mobitz II) has a slower heart rate than the underlying rhythm, plus regular P waves and occasionally absent QRS complexes. PR interval is usually normal and constant, and the QRS complex is consistent in shape
• Second-degree AV block etiology involves a P wave generated without being conducted to the ventricles
• Causes includes heart disease, increased vagal tone, conduction system disease, ablation of the AV node, and inferior/right ventricular MIs
• Clinical manifestations may be asymptomatic or include symptoms if frequent beats are missed
• Medical management involves a potential pacemaker
• Third-degree AV block has an atrial rate (normal) and a ventricular rate (20-40 bpm) The P-P and R-R intervals are regular, but there's no relationship between P waves and QRS complexes; measurable PR interval and a typically widened QRS complex
• The atria and ventricles beat independently in Third-degree AV block etiology
• Causes can include ischemic heart disease, acute MI, and conduction system disease
• Clinical manifestations typically include symptoms of decreased cardiac output
• Medical management often includes some kind of pacing intervention

Ventricular Rhythms

• Premature Ventricular Contractions (PVCs) occur with a rhythm interrupted by the premature beat, an unmeasurable PR interval, and a wide/bizarre QRS complex (>0.12 seconds)
• Etiology is associated with abnormal ventricle beats
• Causes include hypoxemia, ischemic heart disease, hypokalemia, hypomagnesemia, increased catecholamine levels, and digitalis toxicity
• Clinical manifestations include palpitations and signs of decreased cardiac output
• Medical management includes addressing the underlying cause; beta-adrenergic blockers, antianginas, or antidysrhythmics
• Ventricular Tachycardia (V-Tach) has a rate of 110-250 bpm with a regular rhythm, an absent PR interval, and a QRS complex >0.12 seconds

Ventricular Tachycardia Etiology

• Ventricular Tachycardia originates from three or more successive PVCs from a single ectopic focus in the ventricles
• Causes include acute MI, hypoxemia, metabolic acidosis, electrolyte disturbances, and drug toxicity
• Clinical manifestations include a possible pulse and blood pressure; symptoms of low cardiac output; and cardiac arrest if no pulse.
• Medical management includes procainamide, amiodarone, lidocaine (if due to ischemia), cardioversion (if a pulse is present), and ACLS (if no pulse)
• Ventricular Fibrillation (V-Fib) has rate that is non-discernible, a rhythm that is non-discernible, and no interval measurements. Shape/sequence are wavy/chaotic.

Ventricular Fibrillation Etiology

• Ventricular Fibrillation involves a chaotic rhythm with quivering ventricles
• Causes can include ischemia from MI, valvular heart disease, electrolyte and acid-base imbalances, and QT prolongation from medications
• Clinical manifestations include loss of consciousness and pulse, no respirations or blood pressure, seizures, and death
• Medical management includes emergency treatment with CPR, defibrillation, epinephrine, and vasopressin or amiodarone

Assessment and Diagnosis of Dysrhythmias

• Subjective assessment of dysrhythmias include patient reports of palpitations, skipped beats, nausea, light-headedness, vertigo, anxiety, dyspnea, fatigue, and chest discomfort
• Objective assessment of dysrhythmias may include ECG monitoring, syncope, irregular pulse, tachycardia, and tachypnea
• Diagnostic tests used to detect dysrhythmias include ECG / Holter monitoring, telemetry, cardiac catheterization

Nursing Interventions and Patient Teaching

• Nursing assessment of dysrhythmias includes taking apical pulse for a full minute and assessing the patient's anxiety and understanding
• Nursing interventions for dysrhythmias includes monitoring heart rate/rhythm, assessing tissue perfusion, administering oxygen/anti-dysrhythmic medications, reducing cardiac workload, elevating the head of bed, teaching relaxation techniques, providing position changes/support, notifying the physician of chest pain, allowing patients to verbalize their fears/emotions, and reassuring patients supervised
• Patient teaching for dysrhythmias includes medication education, demonstrating how to palpate and count the radial pulse, importance of avoiding tobacco and stimulants, energy conservation, exercise program, and stress management

Cardioversion

• Cardioversion is the synchronized delivery of a shock to disrupt ectopic pacemakers
• Cardioversion allows the SA node to regain control of the rhythm
• Cardioversion is used for tachydysrhythmias (VT, atrial flutter, atrial fibrillation, or supraventricular tachycardia) with a pulse, but developing symptoms
• Requires a rapid response for unstable patients to reduce risk
• Is scheduled for stable patients who are not developing symptoms or any significant risk factors
• Before starting cardioversion, prepare the patient, hold digitalis/diuretics, obtain an ECG, remove dentures, ensure informed consent, start an IV
• After cardioversion, monitor vital signs, cardiac rhythm, plus repeat ECG

Pacemakers

• Pacemakers are battery-operated devices that initiate and control heart rate.
• Pacemakers are used for bradydysrhythmias, tachydysrhythmias, or AV blocks not treatable with medications
• Nursing interventions for pacemakers include monitoring the heart rate and rhythm; checking vital signs and LOC; checking the insertion site for infection; and immobilizing the affected arm
• Patient education for pacemakers involves instructing the patient to wear Medic-Alert/carry a pacemaker information card; report adverse signs and symptoms; take their daily radial pulse; avoid holding electrical appliance/being near large magnetic fields